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CASE DESCRIPTION

A 50-year-old man presented to the emergency department with a 5-day history of a sore throat, progressive hoarseness pyrexia, odynophagia, and a dry, nonproductive cough. Symptoms of stridor and dyspnea had developed rapidly over the preceding 24 hours. Collateral history alleged that he had been smoking crack cocaine 2 days before admission.

In the emergency department, the patient had a respiratory rate of 35 breaths per minute and stridor. He received oxygen via facemask, cefotaxime, nebulized epinephrine, and IV dexamethasone. Two hours after the initial treatment, his oxyhemoglobin saturation (SpO2) intermittently decreased to a nadir of 64%. Arterial blood gases while breathing 4 L oxygen via mask were PaO2 of 56 mm Hg and PaCO2 of 19 mm Hg.

On our arrival, the patient was sitting upright, appeared distressed, was drooling, unable to speak in full sentences, and had appreciable stridor. His SpO2 varied between 77% and 85%, mean arterial blood pressure was 62 mm Hg, and heart rate was 125 bpm. Immediate resuscitation was commenced with 15 L oxygen via a nonrebreathing mask. Preparations for emergency tracheal intubation were made because our opinion was that the patient was in extremis. After administration of 100% oxygen via a Mapleson-C circuit with continuous positive airway pressure of 8 cm H20, the patient’s condition appeared to have improved, with his SpO2 remaining above 90%. He was transferred to the ITU for further airway management and monitoring.

In the ITU, with both a senior anesthesiologist and ear, nose, and throat surgeon nearby, after a burst of nebulized epinephrine and 8 mg IV dexamethasone, NIPPV was begun, with an intermittent positive airway pressure of 12 cm H2O, an expiratory positive airway pressure of 4 cm H2O, along with intermittent nebulized epinephrine and oral mouth care.

The patient’s condition substantially improved over the ensuing 8-hour course of NIPPV. This was evident by: SpO2 and arterial oxygen partial pressures remaining within normal limits; apparent marked reduction in work of breathing; no longer feeling breathless; and able to talk in full sentences. Flexible nasal endoscopy confirmed a working diagnosis of suppurative epiglottitis and supraglottitis, with the presence of notable upper airway edema. The patient was monitored for 24 hours in the ITU and successfully discharged home several days later. Blood tests revealed leukocytosis with neutrophilia, and cultures taken from the epiglottis and blood failed to identify a causative pathogen.

DISCUSSION

AAE is defined as the inflammation of the epiglottis along with the adjacent supraglottic structures, including the vallecula, arytenoids, and aryepiglottic folds.1 The incidence of AAE is 1 to 4 per 100 000,2 with prevalence decreasing since the introduction of the Hemophilus influenzae type-b vaccination in 1992.2,3 AAE has surreptitiously become a disease of adulthood, and unlike that in children, the etiology is often multifaceted.2 In adults, the most common pathogen is H influenzae, followed by other bacteria (H. parainfluenzae, Streptococcus pneumoniae, and Lancfield group A streptococci) viruses (herpes simplex virus) and fungi (Candida and Aspergillus).4 Noninfective causes include thermal injuries (e.g., from crack cocaine or marijuana inhalation), caustic chemical insults, and foreign body inhalation.3,4

Patients with AAE typically present with symptoms of sore throat, fever, and vocal changes (muffled, or hoarse voice).4,5 In contrast to children, the onset of symptoms are usually indolent.4 Drooling and stridor are uncommon; their presence suggesting increased severity, ensuing respiratory compromise, and ultimately predictors of airway loss.5–7 Friedman et al.4 called for a harmonization on the classification of AAE, subsequently categorizing it into 4 stages, depending on severity of respiratory compromise (Table 1).

Indirect laryngoscopy may be used to confirm the diagnosis. There is often extensive swelling of the aryepiglottic structures and loss of the valecullar air space.2,7 The hallmark “cherry-red” epiglottis occurring in children may be absent in AAE.7,8 Lateral neck soft tissue radiographs may also help to confirm diagnosis, by delineating an enlarged (>8 mm) epiglottis, the “thumb-print sign” (Fig. 1).2

The treatment of epiglottitis centers on airway management and early microbial therapy (unless the history suggests the etiology is unlikely to be infective). In contrast to pediatric patients, conservative management is advocated by most authors. Nebulized epinephrine, as used in this patient, albeit widely used, lacks any credible evidence base in AAE2 (juxtaposed to viral croup). The role of corticosteroids is controversial, with the theoretical effects of reduction in airway edema (thereby increasing airway caliber), failing to be validated by large studies.1,6 Corticosteroids have been ascribed to show no benefit to morbidity and mortality, and Rivron and Murray5 associated the use of corticosteroids with worse outcome.1,6

NIPPV for type ΙΙ, lower respiratory tract failure has been well documented, with level “1a” evidence from systematic reviews of randomized control trials.8,9 The evidence for type Ι respiratory failure is somewhat mixed and varies depending on the underlying etiology.

The use of NIPPV for stridor has few reports in the literature, with almost all accounts being reported in children. Namachivayam et al.8 reported that over a 30-year period the use of NIPPV (including nasal continuous positive airway pressure) for stridor had reduced the rate of tracheal intubation, length of intensive care stay, and subsequent mortality. Despite the many benefits of NIPPV in both type 1 and type 2 respiratory failure, clinicians should be mindful that these measures may fail, and formal tracheal intubation may become mandatory. In cases such as AAE, anesthesiologists, due to their advanced airway skills, familiarity with potentially difficult airways, and unique ability to stabilize critically ill patients, are principally trained to manage such rapidly evolving airway emergencies.

In summary, AAE is a rare but potentially fatal airway emergency mandating early involvement by experienced anesthesiologists and an ear, nose, and throat surgeon because airway loss can be sudden and cataclysmic. Severe cases must be transferred to and stabilized in an appropriately monitored environment, with provision for rescue (including surgical) intervention.

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